Bone loss as a result of immobilisation is well established. The available literature suggsests that recovery of bone losses either after clinical immobilisation (LeBlanc & Schneider, 1991) or space flight (Vico et al., 2000) is rather incomplete. For the first time, we ventured to find out whether bone losses acquired during bed rest can recover. Twenty-five male healthy participants (23 to 41 years old) underwent -6 deg head down tilt bed rest for 90 days. Bone mineral content (BMC) of the tibia was measured during bed rest and during 360 days follow up by peripheral Quantitative Computed Tomography (XCT2000, Stratec, Germany). On the 89th day of bed rest, changes in BMC ranged between -15.6% and +0.3% (mean -3.5%, SD 3.6%) at the tibia epiphysis and between -3.5% and +0.7% (mean -0.8%, SD 1.1%) at the diaphysis. After 360 days of recovery, the diaphysis had fully recovered. At the epiphysis, there was still a loss by 0.6% in BMC (SD 1.3%, p = 0.03). These residual losses were independent of the participants’ age and of initial losses at the end of BR (p>0.45). However, a repeated measures ANOVA yielded gains by 0.7% (SD 0.9%) in BMC between 180 and 360 days of recovery (p 80%) in the epiphysis, where recovery seemed to be still ongoing after one year. Moreover, those individuals who lost larger amounts during bed rest depicted larger gains in the recovery period, implying that more or less the same amounts were recovered that had previously been lost. In an extreme case, 17.1% in epiphyseal BMC were gained during recovery, demonstrating the adult skeleton’s ability to accrue bone mass at a rate exceeding that during the pubertal growth spurt. On the other hand, the largest individual change from baseline amounted to 1.9%. These findings clearly demonstrate that the adult skeleton retains a considerable capability of gaining bone mass, which is in contrast to the inefficiency of exercise to increase bone mass normally seen in adults. On the other hand, we found the ‘peak bone mass’ to be tightly regulated in our study. We would therefore argue that bone strength, including its age-related changes, are regulated by factors outside the bone.